Toxic Alcohol Poisoning and Metabolic Acidosis

Toxic alcohol ingestion remains a significant global health concern owing to its rapid conversion into potent acids that disrupt metabolic homeostasis. Substances such as methanol, ethylene glycol and isopropanol undergo enzyme-mediated oxidation, yielding metabolites—formic acid from methanol and glycolate and oxalate from ethylene glycol—that precipitate high anion gap metabolic acidosis. Clinical manifestations range from gastrointestinal upset and central nervous system depression to visual disturbances, acute kidney injury and cardiopulmonary compromise. The degree of acidaemia, often assessed by serum pH and bicarbonate levels, correlates closely with morbidity and mortality. Rapid recognition of toxic alcohol poisoning is critical, combining suspicion based on history, the presence of an increased osmolar gap and anion gap, and specific laboratory measurements. Management strategies centre on inhibition of alcohol dehydrogenase activity through antidotes such as fomepizole or ethanol, correction of acid–base derangements, and removal of parent compounds and metabolites via extracorporeal treatments such as intermittent haemodialysis. Emerging protocols emphasise individualised thresholds for intervention and ongoing monitoring of metabolic indicators to guide the duration of therapy and prevent long-term sequelae, particularly optic neuropathy and renal impairment.

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Toxic Alcohol Poisoning and Metabolic Acidosis publication trend

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Technical terms

Anion gap: The calculated difference between serum cations (sodium plus potassium) and anions (chloride plus bicarbonate), used to detect unmeasured acids in metabolic acidosis.

Osmolar gap: The disparity between measured serum osmolality and calculated osmolarity, indicative of the presence of low-molecular-weight toxins.

Metabolic acidosis: A state characterised by decreased blood pH and bicarbonate concentration due to accumulation of acids or loss of bicarbonate.

Extracorporeal treatment: Therapeutic procedures such as intermittent haemodialysis that remove toxins and correct acid–base disturbances by circulating blood outside the body through specialised filters.

Fomepizole: A competitive inhibitor of alcohol dehydrogenase that prevents the formation of toxic metabolites in methanol and ethylene glycol poisoning.

Formic acid: The primary toxic metabolite of methanol responsible for inhibition of mitochondrial respiration and optic nerve injury.

References

1. Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup. Critical Care (2023).
2. Methanol poisoning as a new world challenge: A review. Annals of Medicine and Surgery (2021).
3. Methanol-induced optic neuropathy: a still-present problem. Archives of Toxicology (2022).
4. A Systematic Review of Ethanol and Fomepizole Use in Toxic Alcohol Ingestions. Emergency Medicine International (2013).